Mayo Clinic researchers have reported a causal link between senescent cells — the cells associated with aging and age-related disease — and bone loss in mice. Targeting these cells led to an increase in bone mass and strength. The findings appear online in Nature Medicine.
Low bone mass and osteoporosis are estimated to be a major public health threat for almost 44 million U.S. women and men 50 and older, according to the National Osteoporosis Foundation. Bone is a living tissue that is constantly being broken down and replaced. Osteoporosis occurs when the creation of new bone doesn’t keep up with the removal of old bone.
“While we know from previous work that the accumulation of senescent cells causes tissue dysfunction, the role of cell senescence in osteoporosis up to this point has been unclear,” says Sundeep Khosla, M.D., director of the Aging Bone and Muscle program at Mayo Clinic’s Robert and Arlene Kogod Center on Aging. “The novelty of this work for the bone field lies in the fact that, rather than targeting a bone-specific pathway, as is the case for all current treatments for osteoporosis, we targeted a fundamental aging process that has the potential to improve not only bone mass, but also alleviate other age-related conditions as a group.”
In the study, researchers used multiple approaches to target senescent cells in mice with established bone loss between 20 and 22 months of age. That’s the equivalent of over age 70 in humans. Approaches included using:
- A genetic model where senescent cells can be killed off
- A pharmacological approach, where senolytic drugs previously developed at Mayo Clinic eliminate senescent cells
- A Janus kinase inhibitor — a drug that blocks the activity of Janus kinase enzymes — to eliminate the toxic products produced by senescent cells
